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. 2021 Feb 12:17:37-47.
doi: 10.2147/VHRM.S290841. eCollection 2021.

Rapid Rise of Cardio-Ankle Vascular Index May Be a Trigger of Cerebro-Cardiovascular Events: Proposal of Smooth Muscle Cell Contraction Theory for Plaque Rupture

Kazuhiro Shimizu  1 , Mao Takahashi  1 , Shuji Sato  1 , Atsuhito Saiki  1 , Daiji Nagayama  1 , Masashi Harada  2 , Chikao Miyazaki  2 , Akira Takahara  3 , Kohji Shirai  1
Affiliations

Rapid Rise of Cardio-Ankle Vascular Index May Be a Trigger of Cerebro-Cardiovascular Events: Proposal of Smooth Muscle Cell Contraction Theory for Plaque Rupture

Kazuhiro Shimizu et al. Vasc Health Risk Manag. .

Abstract

Cardiovascular diseases have been recognized as the main cause of death all over the world. Recently, the established cardio-ankle vascular index (CAVI) has become known as an index of arterial stiffness of the arterial tree from the origin of the aorta to the ankle. CAVI reflects the progress of arteriosclerosis, and a rapid rise in CAVI indicates arterial smooth muscle cell contraction. Considering the vasculature of the atheroma where vasa vasorum penetrates the smooth muscle cell layer and supplies blood to the intimal atheromatous lesion, a rapid rise of CAVI means "choked" atheroma. Thus, we proposed a "smooth muscle cell contraction" hypothesis of plaque rupture.

Keywords: CAVI; arterial stiffness; atherosclerosis; smooth muscle cell contraction.

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Conflict of interest statement

The authors report no conflicts of interest related to this work.

Figures

Figure 1
Figure 1
Increase in cardio-ankle vascular index (CAVI) just after the Great East Japan Earthquake (M9; March 11, 2011). The immediate increase was seen in both healthy young adults and in coronary artery disease (CAD) patients, despite their relatively stable blood pressure (A). Some patients showed a marked increase in CAVI following the earthquake, such as in the CAVI results of the diabetic hypertense patient shown here (B) who suffered psychological stress.
Figure 2
Figure 2
Increase in the cardio-ankle vascular index (CAVI) prior to cerebro-cardiovascular events. Cases with a rapid rise in CAVI who had acute myocardial infarction 4 months later (A), cerebral hemorrhage 7 days later (B), and aortic dissection 2 weeks later (C).
Figure 3
Figure 3
Increase in cardio-ankle vascular index (CAVI) over 13 years in an atherosclerosis patient with a high baseline CAVI. This patient showed a rapid rise in CAVI (to 11.5) a few months before cerebral infarction and a high rapid rise to 12.8 just prior to cerebral hemorrhage.
Figure 4
Figure 4
Carotid endarterectomy of a patient with 90% stenosis of the cervical artery. (A) Atherosclerosis of the carotid artery and endarterectomy; (B) Gauze was applied for the bleeding which occurred after peeling off the intimal atheromatous layer of the carotid artery; (C) Gauze, dipped in the catecholamine noradrenaline, was applied and inhibited the bleeding, indicating that the blood supply of the intimal atheromatous lesion was from the vasa vasorum and that it was stopped by contraction of the medial smooth muscle cells.
Figure 5
Figure 5
“Smooth muscle cell contraction” hypothesis for plaque rupture.
See this image and copyright information in PMC

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